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Background <p>We investigated the serial mediating roles of insulin re-sistance (IR) and abdominal obesity in the association between the Dietary Inflamma-tory Index (DII) and hyperuricemia (HUA), and whether abdominal obesity moder-ated this pathway.</p> Methods <p>We analyzed data from 8,232 adults in the National Health and Nutrition Examination Survey (2007–2016). The triglyceride-glucose (TyG) index served as a surrogate for IR. We employed serial mediation and moderated me-diation models.</p> Results <p>Higher DII was associated with increased HUA risk. This re-lationship was serially mediated through the pathway: DII → TyG index → abdominal obesity → HUA. This indirect pathway accounted for 52.3% of the total effect, with abdominal obesity being the most potent mediator (contribution: 31.0%). Importantly, the mediating effect of the TyG index was significant only in individuals with a normal waist circumference (β = 0.0016, 95% CI: 0.0006, 0.0026) but was attenuated to non-significance in those with abdominal obesity.</p> Conclusion <p>Our findings suggest that IR and abdominal obesity may serially mediate the link between a pro-inflammatory diet and HUA. The me-diating role of IR appears to be prominent in individuals without abdominal obesity, whereas in those with obesity, obesity itself becomes the dominant factor. However, given the cross-sectional design, causal inferences cannot be drawn. These findings support developing stage-specific HUA prevention strategies, targeting insulin sensitivity or weight control based on an individual’s obesity status.</p>

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The link between dietary inflammation and hyperuricemia: what is the mediating role of insulin resistance and abdominal obesity?

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月29日

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  • Weili Liu,
  • Chuyan Feng,
  • Lin Yang,
  • Ke Li

摘要

Background

We investigated the serial mediating roles of insulin re-sistance (IR) and abdominal obesity in the association between the Dietary Inflamma-tory Index (DII) and hyperuricemia (HUA), and whether abdominal obesity moder-ated this pathway.

Methods

We analyzed data from 8,232 adults in the National Health and Nutrition Examination Survey (2007–2016). The triglyceride-glucose (TyG) index served as a surrogate for IR. We employed serial mediation and moderated me-diation models.

Results

Higher DII was associated with increased HUA risk. This re-lationship was serially mediated through the pathway: DII → TyG index → abdominal obesity → HUA. This indirect pathway accounted for 52.3% of the total effect, with abdominal obesity being the most potent mediator (contribution: 31.0%). Importantly, the mediating effect of the TyG index was significant only in individuals with a normal waist circumference (β = 0.0016, 95% CI: 0.0006, 0.0026) but was attenuated to non-significance in those with abdominal obesity.

Conclusion

Our findings suggest that IR and abdominal obesity may serially mediate the link between a pro-inflammatory diet and HUA. The me-diating role of IR appears to be prominent in individuals without abdominal obesity, whereas in those with obesity, obesity itself becomes the dominant factor. However, given the cross-sectional design, causal inferences cannot be drawn. These findings support developing stage-specific HUA prevention strategies, targeting insulin sensitivity or weight control based on an individual’s obesity status.